The ideal of cancer therapy is to promote apoptosis of cancer cells. Traditional chemotherapeutic agents (first generation indirect apoptogens) trigger events which result in apoptosis of cancer cells.
Online PR News – 06-April-2010 – – DALLAS
Biotech-Market-Reports Announce it Will Carry the Apoptosis 2009 Opportunities in Cancer and Other Diseases Market Research Report in its Store.
Browse the complete Report on: http://www.biotech-market-reports.com/market-reports/apoptosis-2009-opportunities-in-cancer-and-other-diseases/
The main application of apoptosis research is presently in cancer treatment. It should be noted that this market is one of the largest and fastest growing sectors of the pharma industry. Of the 370 pipeline agents identified in Apoptosis 2009: Opportunities in Cancer and Other Diseases, 80% are anticancers. This report segments the apoptosis-related cancer market into: direct apoptogens (apoptosis-inducing drugs known, during their development, to have apoptosis-related molecular targets)
a. first generation indirect apoptogens (established drugs such as cytotoxics which have turned out to rely on apoptosis for part of their efficacy)
b. second generation indirect apoptogens (recently introduced and pipeline drugs with non-apoptotic targets which nevertheless have apoptotic effects).
c. Opportunities for apoptosis modulators in indications such as CNS disorders and chronic inflammation/autoimmunity are also explored.
Examination of the molecular events in apoptosis which may become dysregulated, providing opportunities for therapeutic intervention.
• Description of morphological criteria for detecting apoptosis, as well as recent methodologies based on detecting specific biological aspects and biomarkers.
• Analysis of 370 apoptosis-modulating drug candidates (9% in Phase 3 or later) from 233 originating companies. These drugs target 148 known gene targets, of which the top 15 are shown in Figure 1.3 from the report, as reproduced below.
• Deployment of Stanford Research Institute's PANTHER Classification System to identify gene targets with a validated role in apoptosis.
• Analysis of 4,872 apoptosis-related patents and patent applications to identify technology trends and potential therapeutic applications.
• Forecasts for the overall oncology-based apoptosis market, and its individual sectors.
Utilize biomarker and drug target information in this report to discover and develop drugs with apoptosis-modulating properties.
• Identify emerging areas of opportunity for apoptosis modulators in cancer, CNS diseases, and chronic inflammation/autoimmunity.
• Gain up-to-date competitive intelligence on apoptosis-modulating pipelines and identify the most promising drugs under development.
• Identify the leading originator companies developing apoptosis-modulating drugs.
Use the patent analysis presented in this report to identify leading assignees, most influential patents and unexploited indications for apoptosis modulation.
• Devise a commercial strategy leveraging apoptosis by utilizing market forecasts for the oncology-based apoptosis market to 2013.
Key Issues raised
The ideal of cancer therapy is to promote apoptosis of cancer cells. Traditional chemotherapeutic agents (first generation indirect apoptogens) trigger events which result in apoptosis of cancer cells. However, they also kill normal cells. Second generation indirect apoptogens may be less toxic to normal cells.
• Wide prevalence of indirect apoptotic effects suggests that it is always worth screening for apoptotic effects of new anticancer drugs. Wider application of validated biomarkers of apoptosis in preclinical and clinical trials of new drugs is thus highly desirable.
• The utility of current anticancer therapies is limited by drug resistance, either intrinsic or acquired. Direct apoptogens target overexpressed anti-apoptotic proteins or downregulated pro-apoptotic proteins responsible for therapy resistance.
• Neurodegenerative diseases represent an area of unmet clinical need. No therapy for neuroprotection is currently marketed, but new apoptosis-modulating drugs in development show promise.
• Existing treatments for rheumatoid arthritis and other autoimmune conditions (anti-TNF therapies and glucocorticoids) may act partly via apoptosis modulation. However, new apoptosis- modulating therapies with improved specificity are needed.
In our survey of the apoptosis drug landscape, we identified 370 drugs aimed at 148 known gene targets.HSP90 (heat shock protein 90) is numerically the most popular target overall.
Seventy-six percent of all apoptosis-modulating drugs in development are anticancers, including 27 radio/chemosensitizers (7%). The overall apoptosis market is forecast to grow from $28 billion in 2008 to $57 billion in 2013.
• Of particular interest are first-in-class direct apoptogens (over 100 agents identified) which target elements of the apoptotic pathway (over 40 genes). The global market for direct apoptogens is forecast to grow from $606 million in 2008 to $12 billion in 2013.
• The leading subgroups of the direct apoptogens market are: proteasome inhibitors; modulators of heat shock proteins; TP53-targeted agents; caspase-targeted agents: BCL2-targeted agents; and multi-target apoptogens.
• Eighteen percent (65) of all apoptosis-modulating drugs in development are anti-inflammatory, and 6% (24) are CNS targeted. Our survey of apoptosis-related patents suggests that future drugs will also target infectious disease.
Key Questions answered
• What types of apoptosis-modulating drugs are on the market?
• Which companies are leading the way in the development of apoptosis- modulating drugs?
• Which assays and biomarkers are increasingly used to define apoptosis during drug development?
• Why should all new anticancer drugs be screened for apoptotic effects?
• How is the apoptosis drug target landscape shaping up?
• What are the most popular targets of direct apoptogens in development for the treatment of cancer?
• How is the global cancer apoptosis market segmented and how are these sectors expected to perform over the period 2008-13?
• What progress is being made in developing apoptosis-modulating drugs for the treatment of CNS diseases and inflammation/autoimmunity?
• What is the nature of the apoptosis-related patent landscape?
Table of Content
List of Tables and Figures
About the Authors
Chapter 1 Apoptosis and its regulation
1.0 Chapter summary
1.1 Introduction to apoptosis
1.2 Apoptosis versus necrosis
1.3 Other modes of cell death
1.3.2 Mitotic catastrophe
1.4 Mechanisms of apoptosis
1.5 Key molecular players in apoptosis
1.5.1 TNF family and death receptors
1.5.2 Apoptosis adaptor proteins
1.5.3 Caspases and other proteases
1.5.4 BCL2 family
1.5.5 IAPs and other regulators of caspases
1.5.6 Intracellular kinases
1.5.7 Transcription factors and regulators
1.6 Apoptotic pathways
1.6.1 Extrinsic pathway
1.6.2 Intrinsic pathway
1.6.3 The perforin/granzyme pathway
1.6.4 Execution pathway
1.7 Targeting dysregulated apoptosis
1.8 Apoptosis pipeline audit
Chapter 2 Assays and biomarkers of apoptosis
2.0 Chapter summary
2.2 Analysis of cytomorphological parameters
2.3 Analysis of mitochondrial parameters
2.4 Biomarker-based assays of apoptosis
2.4.1 Commonly assayed biomarkers
184.108.40.206 Externalized phosphatidylserine
220.127.116.11 Nucleosomal DNA
18.104.22.168 Cytochrome c
22.214.171.124 Other protein biomarkers
126.96.36.199 Cytokeratins (cancer)
Chapter 3 Indirect apoptogens in development for cancer
3.0 Chapter summary
3.1 Introduction to cancer
3.2 Overview of anticancer pharmacotherapies
3.3 Detecting apoptotic effects of new drugs
3.4 Drugs in development with apoptotic effects
3.5 First generation indirect apoptogens
3.5.1 Radio- and chemo-sensitizers
3.5.2 Alkylating and other DNA-binding agents
3.5.4 Topoisomerase inhibitors
3.5.5 Antitumor antibiotics
3.5.6 Microtubule-targeting agents
3.6 Second generation indirect apoptogens
3.6.1 Hormone antagonists
188.8.131.52 Monoclonal antibodies
184.108.40.206 Non-antisense oligonucleotides
220.127.116.11 Oncolytic viruses
3.6.3 Focus on kinase inhibitors
Chapter 4 Direct apoptogens in development for cancer
4.0 Chapter summary
4.1 Promoting apoptosis of cancer cells
4.2 Gene targets of apoptogens in development
4.2.1 TNF family and death receptors
18.104.22.168.1 Description of target
22.214.171.124.2 Drugs in development
126.96.36.199.1 Description of target
188.8.131.52.2 Drugs in development
184.108.40.206.1 Description of target
220.127.116.11.2 Drugs in development
18.104.22.168.1 Description of target
22.214.171.124.2 Drugs in development
126.96.36.199.1 Description of target
188.8.131.52.2 Drugs in development
184.108.40.206.1 Description of target
220.127.116.11.2 Drugs in development
18.104.22.168.1 Description of target
22.214.171.124.2 Drugs in development
126.96.36.199.1 Description of target
188.8.131.52.2 Drugs in development
4.2.3 BCL2 family
184.108.40.206.1 Description of target
220.127.116.11.2 Drugs in development
18.104.22.168.1 Description of target
22.214.171.124.2 Drugs in development
126.96.36.199.1 Description of target
188.8.131.52.2 Drugs in development
184.108.40.206.1 Description of target
220.127.116.11.2 Drugs in development
4.2.4 IAPs and regulators
18.104.22.168.1 Description of target
22.214.171.124.2 Drugs in development
126.96.36.199.1 Description of target
188.8.131.52.2 Drugs in development
184.108.40.206.1 Description of target
220.127.116.11.2 Drugs in development
18.104.22.168.1 Description of target
22.214.171.124.2 Drugs in development
126.96.36.199.1 Description of target
188.8.131.52.2 Drugs in development
4.2.5 Transcription factors and regulators
184.108.40.206.1 Description of target
220.127.116.11.2 Drugs in development
18.104.22.168.1 Description of target
22.214.171.124.2 Drugs in development
126.96.36.199.1 Description of target
188.8.131.52.2 Drugs in development
184.108.40.206.1 Description of target
220.127.116.11.2 Drugs in development
4.2.6 Kinases in the PI3K/AKT pathway
18.104.22.168.1 Description of target
22.214.171.124.2 Drugs in development
126.96.36.199.1 Description of target
188.8.131.52.2 Drugs in development
184.108.40.206.1 Description of target
220.127.116.11.2 Drugs in development
18.104.22.168.1 Description of target
22.214.171.124.2 Drugs in development
4.2.7 Histone deacetylases
126.96.36.199 HDAC (1-5, -7, -8, and -11)
188.8.131.52.1 Description of target
184.108.40.206.2 Drugs in development
4.2.8 Other targets
4.3 Proteasome inhibitors
4.4 HSP inhibitors
Chapter 5 Other apoptosis modulators in development
5.0 Chapter summary
5.1 CNS diseases
5.1.1 Apoptosis agents in development
220.127.116.11 Apoptosis antagonists
18.104.22.168 Apoptosis agonists
5.2 Chronic inflammation and autoimmunity
5.2.1 Apoptosis agents in development
22.214.171.124 Apoptosis agonists
126.96.36.199 Apoptosis antagonists
5.3 Other apoptosis agents in development
Chapter 6 Commercial Outlook: Patent and Market Analysis
6.0 Chapter Summary
6.1 Patent Analysis
6.1.2 Uses of Patent Information
6.1.3 The Apoptosis Patent Dataset
6.1.4 Apoptosis Patents by Filing and Publication Years
6.1.5 Apoptosis Patents by Leading Assignees
6.1.6 Focus on Cytovia / Maxim / EpiCept
6.1.7 Apoptosis Patents by Forward Citations
6.1.8 Apoptosis Patents by Activity
6.2 Market Analysis
188.8.131.52 Disease burden
184.108.40.206 Anticancer drug landscape
6.2.3 Non-cancer apoptosis modulators
6.2.4 World pharmaceutical market
6.2.5 Market outlook for apoptotic drugs
220.127.116.11 Drug and Target Types
18.104.22.168 Focus on Velcade (bortezomib)
22.214.171.124 Focus on Gendicine
126.96.36.199 Direct apoptogens
188.8.131.52 Indirect apoptogens
Chapter 7 Trends and opportunities
7.0 Chapter summary
7.1 Apoptosis modulation offers varied opportunities
7.2 New directions in cancer drug development
7.3 Combinatorial approaches to cancer drug resistance
7.4 Focus on apoptosis-resistant cancer stem cells
7.5 Key role for biomarkers of apoptosis in cancer
7.6 Prospects for apoptosis modulators in other areas
Appendix 1 Abbreviations and Acronyms
A1.1 Key gene targets for apoptotic modulation
A1.2 Other scientific/medical terms
Appendix 2 Research Methodology
Appendix 3 List of Tables and Figures
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